混合静脉血氧饱和度

混合静脉血氧饱和度

拉丁学名：Oxygen Saturation of Mixed Venose Blood；SvO

2

相关疾病：循环衰竭；败血症；心源性休克；甲亢；贫血及变性血红蛋白症；

脓毒症

【参考值】

68%～77%；平均75%

【临床意义】

通过测定混合静脉血氧饱和度（SvO

2

）来计算动静脉血氧含量差，能较准确反映

心排出量。Waller等曾指出SvO

2

和心脏指数、每搏指数及左心室每搏指数之间

有很高的相关性。SvO

2

下降，而动脉血氧饱和度和耗氧量尚属正常时，则可证明心排血量也是低的。因此现在认为混合静脉血的氧饱和度检查对严重心肺疾患的监测具有重要价值。

SvO

2增高的常见原因是脓毒症，此外氰化物中毒及低温也可使SvO

2

增高。

SvO

2

降低的原因有：心输出量下降导致的血循环量不足、周围循环衰竭、败血症、

心源性休克、甲亢、贫血及变性血红蛋白症、肺部疾患等各种原因导致的氧合

功能减低者。SvO

2

低于60%时，通常提示组织耗氧增加或心肺功能不佳。

临床上连续测定SvO

2

对危重患者的监测起到重要作用，并对治疗方法及药物使用也有一定的指导作用

Nuclear factor kB (NF-kB) is a nuclear transcription factor that regulates expression of a large number of genes that are critical for the regulation of apoptosis, viral replication, tumorigenesis, inflammation, and various autoimmune diseases. The activation of NF-kB is thought to be part of a stress response as it is activated by a variety of stimuli that include growth factors, cytokines, lymphokines, UV, pharmacological agents, and stress. In its inactive form, NF-kB is sequestered in the cytoplasm, bound by members of the IkB family of inhibitor proteins, which include IkBa, IkBb, IkBg, and IkBe. The various stimuli that

activate NF-kB cause phosphorylation of IkB, which is followed by its ubiquitination and subsequent degradation. This results in the exposure of the nuclear localization signals (NLS) on NF-kB subunits and the subsequent translocation of the molecule to the nucleus. In the nucleus, NF-kB binds with a consensus sequence (5'GGGACTTTCC-3') of various genes and thus activates their transcription. IkB proteins are phosphorylated by IkB kinase complex consisting of at least three proteins; IKK1/IKKa, IKK2/IKKb, and IKK3/IKKg. These enzymes phosphorylate IkB leading to its ubiquitination and degradation. Tumor necrosis factor (TNF) which is the best-studied activator binds to its receptor and recruits a protein called TNF receptor death domain (TRADD). TRADD binds to the TNF receptor-associated factor 2 (TRAF-2) that recruits NF-kB-inducible kinase (NIK). Both IKK1 and IKK2 have canonical sequences that can be phosphorylated by the MAP kinase NIK/MEKK1 and both kinases can independently phosphorylate IkBa or IkBb. TRAF-2 also interacts with A20, a zinc finger protein whose expression is induced by agents that activate NF-kB. A20 functions to block TRAF2-mediated NF-kB activation. A20 also inhibits TNF and IL-1 induced activation of NF-kB suggesting that it may act as a general inhibitor of NF-kB activation.

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